MicroRNA‑206 inhibits the proliferation, migration and invasion of colorectal cancer cells by regulating the c‑Met/AKT/GSK‑3β pathway
- Jiayu Lyu
- Yao Sun
- Xizhi Li
- Huili Ma
Affiliations: Department of First General Surgery, The Fifth Hospital of Harbin, Harbin, Heilongjiang 150040, P.R. China, Department of Neurology, General Hospital of Heilongjiang Province Land Reclamation Bureau, Harbin, Heilongjiang 150088, P.R. China, Department of Neurology, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China, Department of Emergency Surgical Trauma Center, Binzhou Medical University Hospital, Binzhou, Shandong 256603, P.R. China
- Published online on: December 23, 2020 https://doi.org/10.3892/ol.2020.12408
Copyright: © Lyu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
An imbalance in microRNA (miRNA/miR) expression is closely associated with tumorigenesis and progression. miR‑206 is downregulated in different types of tumors, including colorectal cancer (CRC). However, the effects of miR‑206 on the progression of CRC, and its underlying molecular mechanisms are yet to be elucidated. The present study aimed to investigate the effects of miR‑206 on the proliferation, migration and invasion of colorectal cancer cells, and determine its potential molecular mechanism. The results of the present study demonstrated that the expression levels of miR‑206 and c‑Met were affected in HCT116 and SW480 cells by transfected with miR‑206 mimic, inhibitor or small interfering RNA‑c‑Met. A dual‑luciferase reporter assay was performed to identify the miRNA targets. Cell proliferation, migration and invasion assays were also performed. The results demonstrated that overexpression of miR‑206 significantly decreased the viability of HCT116 and SW480 cells. The results of the Transwell assay indicated that the cell migratory and invasive abilities were inhibited following transfection with miR‑206 mimic. As a target of miR‑206, knockdown of c‑Met significantly suppressed cell viability, migration and invasion. In addition, c‑Met knockdown or overexpression of miR‑206 inhibited activation of the AKT/GSK‑3β pathway. Collectively, these results suggest that miR‑206 suppresses the proliferation, migration and invasion of CRC cells by targeting the c‑Met/AKT/GSK‑3β pathway.